Proliferative kidney disease (PKD) is one of the most economically important diseases among commercially reared rainbow trout (Oncorhynchus mykiss) in Europe and causes significant losses among Pacific salmon and rainbow trout populations in western North America. The parasite that causes PKD is a poorly understood myxosporean (PKX), presumed but not yet proven to be a member of the family Sphaerosporidae, genus Sphaerospora. The disease occurs in both cultured and feral populations of salmonids that come into contact with a 20-25 μm waterborne infective stage. The disease is often seasonally dependent occurring at water temperatures above 15 °C in the summer and fall months of the year. At permissive water temperatures, the first recognizable vegetative or extrasporogonic stages appear about 10-14 days after exposure to the infective stage. They are initially prominent in the blood sinuses of the kidney, are accompanied by a mild hyperplasia of the interstitial hematopoietic cell populations, and multiply via binary fission, endogeny, and plasmotomy, provoking a strong inflammatory response. This diffuse granulomatous response occurs principally in the kidney but is also seen in the spleen and other organs. The major host cell type involved in the lesion is the macrophage, but lymphocytes are also abundant in close proximity to PKX. As the inflammation progresses (6-8 weeks postexposure to the infective stage), the gross renal swelling becomes evident as do other clinical signs including anemia. Mortality in uncomplicated cases of PKD is generally 20% or less but often secondary pathogens or unfavorable environmental conditions coincide with peak periods of PKD and mortalities can reach 95-100%. Compromised renal functions such as macromolecule adsorption and divalent cation excretion are also impaired and this may contribute to the mortality observed among fish with PKD. Generally, by 12-20 weeks postexposure, fish begin, or are in the process of, recovery and the renal hematopoietic and excretory functions return to normal. In fish that have experienced a full clinical episode of the disease, a strong acquired immunity develops. The basis of the immunity is unknown but circulating antiparasite antibodies can be detected as early as six weeks postexposure to the infective stage. A strong cellular component to the immunity is also suspected. No vaccines have yet been developed to control PKD, and only recently have experimental therapies been applied. Both fumagillin DCH, an antibiotic effective against certain microsporidia and myxosporidia, and the arylmethane dye malachite green, have shown some promise as treatments for PKD. Unfortunately, neither drug is licensed for use in the U.S. and both treatments suffer from potential difficulties with drug toxicity, tissue residues, or durg discharges in hatchery effluent waters.
- Proliferative disease
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